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硫缺乏导致索氏小球藻(211/8k)的氧化扰动。

Sulfur Deprivation Results in Oxidative Perturbation in Chlorella sorokiniana (211/8k).

作者信息

Salbitani Giovanna, Vona Vincenza, Bottone Claudia, Petriccione Milena, Carfagna Simona

机构信息

Dipartimento di Biologia, Università di Napoli Federico II, Via Foria 223, I-80139 Napoli, Italy.

Consiglio per la Ricerca e la Sperimentazione in Agricoltura, Unità di ricerca per la Frutticoltura, Via Torrino 2, 81100 Caserta, Italy.

出版信息

Plant Cell Physiol. 2015 May;56(5):897-905. doi: 10.1093/pcp/pcv015. Epub 2015 Feb 2.

Abstract

Sulfur deficiency in plant cells has not been considered as a potential abiotic factor that can induce oxidative stress. We studied the antioxidant defense system of Chlorella sorokiniana cultured under sulfur (S) deficiency, imposed for a maximum period of 24 h, to evaluate the effect of an S shortage on oxidative stress. S deprivation induced an immediate (30 min) but transient increase in the intracellular H2O2 content, which suggests that S limitation can lead to a temporary redox disturbance. After 24 h, S deficiency in Chlorella cells decreased the glutathione content to <10% of the value measured in cells that were not subjected to S deprivation. Consequently, we assumed that the cellular antioxidative mechanisms could be altered by a decrease in the total glutathione content. The total ascorbate pool increased within 2 h after the initiation of S depletion, and remained high until 6 h; however, ascorbate regeneration was inhibited under limited S conditions, indicated by a significant decrease in the ascorbate/dehydroascorbate (AsA/DHA) ratios. Furthermore, ascorbate peroxidase (APX) and superoxide dismutase (SOD) were activated under S deficiency, but we assumed that these enzymes were involved in maintaining the cellular H2O2 balance for at least 4 h after the initiation of S starvation. We concluded that S deprivation triggers redox changes and induces antioxidant enzyme activities in Chlorella cells. The accumulation of total ascorbate, changes in the reduced glutathione/oxidized glutathione (GSH/GSSG) ratios and an increase in the activity of SOD and APX enzymes indicate that oxidative perturbation occurs during S deprivation.

摘要

植物细胞中的硫缺乏尚未被视为一种能够诱导氧化应激的潜在非生物因素。我们研究了在硫(S)缺乏条件下培养的索氏小球藻的抗氧化防御系统,硫缺乏的最长时间为24小时,以评估硫短缺对氧化应激的影响。硫剥夺导致细胞内过氧化氢含量立即(30分钟)但短暂增加,这表明硫限制可能导致暂时的氧化还原紊乱。24小时后,小球藻细胞中的硫缺乏使谷胱甘肽含量降至未经历硫剥夺的细胞中测量值的<10%。因此,我们认为细胞抗氧化机制可能会因总谷胱甘肽含量的降低而改变。在开始硫消耗后2小时内,总抗坏血酸库增加,并在6小时内保持高水平;然而,在硫有限的条件下,抗坏血酸再生受到抑制,抗坏血酸/脱氢抗坏血酸(AsA/DHA)比值显著下降表明了这一点。此外,在硫缺乏条件下,抗坏血酸过氧化物酶(APX)和超氧化物歧化酶(SOD)被激活,但我们认为这些酶在硫饥饿开始后至少4小时内参与维持细胞过氧化氢平衡。我们得出结论,硫剥夺会引发氧化还原变化并诱导小球藻细胞中的抗氧化酶活性。总抗坏血酸的积累、还原型谷胱甘肽/氧化型谷胱甘肽(GSH/GSSG)比值的变化以及SOD和APX酶活性的增加表明,在硫剥夺期间会发生氧化扰动。

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